CD34 expression is regulated reciprocally with adhesion molecules in vascular endothelial cells in vitro

Abstract

Freshly cultured vascular endothelial cells express the CD34 antigen in a diffuse cell surface pattern with some concentration on microvilli. Expression is downregulated with proliferation in continuous culture and undetectable after nine population doublings but can be maintained by restraining cell proliferation and promoting cell contact. Expression of CD34 at the antigen and mRNA levels on early passage cells is rapidly downregulated by interleukin-1 beta (IL-1 beta), interferon-gamma (INF-gamma), and tumor necrosis factor-alpha (TNF- alpha) under conditions in which these ligands upregulate the adhesion molecules: endothelial leukocyte adhesion molecule 1 (ELAM-1) and intracellular adhesion molecule 1 (ICAM-1). This reciprocal pattern of expression and the topographic distribution of CD34 molecules on the lumenal interdigitated microprocesses of adjacent endothelial cells in vivo suggest that CD34 might have a negative modulating role on adhesion functions of endothelia.

Microvesicles produced by natural killer cells of the NK-92 cell line affect the phenotype and functions of endothelial cells of the EA.Hy926 cell line

“…A decrease in the expression of CD105 by ECs indicates both shedding of this protein from the cell surface and a decrease in EC sensitivity to the inhibitory effect of TGF-β [38]. Change in the intensity of CD34 and CD54 expression by ECs argues for EC activation [14,31]. During EC culturing with MVs derived from cells of the NK-92 cell line, a dose-dependent decrease in EC proliferation compared with ECs cultured in a medium without MVs was shown.…”

Analysis of Body-wide Unfractionated Tissue Data to Identify a Core Human Endothelial Transcriptome

“…Although cultured venous and arterial ECs can retain distinct gene expression differences, even after multiple passages (Chi et al, 2003), the absence of microenvironment cues, e.g., shear stress, can modulate mRNA levels (Amaya et al, 2015) and stability (Wu et al, 2011), inducing a rapid gene expression drift (Durr et al, 2004;Lacorre et al, 2004). Thus, the loss of pan EC-enriched gene expression in vitro could be due to culture and/or repeated passage, as for CD34 (Delia et al, 1993).…”

Immunolocalization of CD34 in Nasal Polyposis

“…The expression of CD34 is not restricted to hemopoietic progenitor cells, but has also been detected by immunohistochemical analysis on vascular endothelium of normal and neoplastic tissues (29)(30)(31)(32)(33)(34). It has also been shown that the relevant endothelial cells produce the same size protein (MW ϭ 110 kD) and express identical CD34 messenger RNA (2.3 kb) to that expressed by hemopoietic cells, indicating that CD34 antibodies bind to the CD34 gene product on endothelial cells, and not to a cross-reactive epitope (30).…”